| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Source | Plant — Amaryllidaceae Narcissus poeticus L. |
| Molecular weight | |
| Molecular formula | C16H17NO4 |
| SMILES | |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Pancracine is an alkaloid that upregulates p27, phosphorylated p38 MAPK and phosphorylated p53 while downregulating phosphorylated Akt and phosphorylated Rb, inducing G1 cell cycle arrest and apoptosis in cells. It also inhibits replication of pseudotyped HIV-1 and Dengue virus, and can be used in research on lung adenocarcinoma, acute lymphoblastic leukemia, cutaneous epidermoid carcinoma, HIV infection and dengue virus infection[1][2].
It has the molecular formula C16H17NO4 and a molecular weight of 287.31 g/mol.
Physical & Chemical Properties
| CAS Number | 21416-14-8 |
|---|---|
| Molecular Formula | C16H17NO4 |
| Molecular Weight | 287.31 g/mol |
| Structure Classification | Alkaloids Other Alkaloids |
| SMILES | O[C@H]1C=C2[C@]3([H])C4=CC(OCO5)=C5C=C4C[N@]([C@@]2([H])C[C@@H]1O)C3 |
| Target | HIV-1 |
| Signaling Pathway | MAPK/ERK Pathway; Apoptosis; PI3K/Akt/mTOR; Anti-infection |
| Initial Source | Plant — Amaryllidaceae Narcissus poeticus L. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
Pancracine (1-50 μM; up to 96 h) reduces proliferation of A549, MCF-7, HepG2 and A2780 cells with increasing concentration, and 20 μM fully halts A549 cell proliferation for up to 96 h[1]. At concentrations ≥2.5 μM, Pancracine (2.5-20 μM; 24-72 h (A549); 24-48 h (MOLT-4)) has significant antiproliferative effects on A549 and MOLT-4 cells; MOLT-4 cells lose viability more readily than A549 cells under Pancracine[1]. Pancracine (0.5-10 μM; 24 h) shows selective cytotoxicity toward the epidermoid cancer cell line A431[2]. In THP-1 acute monocytic leukemia cells, Pancracine (0.05-200 μM) is cytotoxic, with a CC50 value of 25.93 μM[2]. In A549 cells, Pancracine (2.5-20 μM; 24-48 h) causes G1 phase arrest at 5 μM for 24 h and a shift to G2 phase arrest at 20 μM for 48 h; at higher concentrations and longer incubation times, the proportion of S phase cells also falls[1]. Pancracine (10-20 μM; 24-72 h) inhibits A549 cell proliferation through the Akt/p27/pRb and p38 MAPK/ERK signaling pathways; at ≥10 μM with 72 h of treatment, p38 MAPK phosphorylation and p27 level rise, while ERK and pRb phosphorylation and Akt phosphorylation fall[1]. In MOLT-4 cells, Pancracine (2.5-10 μM; 24-48 h) causes G1 phase arrest and enlarges the sub-G1 apoptotic cell population. A significant G1 phase shift appears after 24 h at 2.5 μM and after 48 h at 5 μM, and sub-G1 apoptotic cells rise dose-dependently[1]. Pancracine (5-20 μM) markedly raises caspase-3/7, -8, and -9 activities in MOLT-4 cells at ≥10 μM after 24 h of treatment, whereas caspase activation is not induced in A549 cells[1]. Pancracine (2.5-20 μM; 24 h) triggers dose-dependent apoptosis in MOLT-4 cells at 24 hours; with 20 μM Pancracine, apoptotic cells reach 48% in total (14% early apoptosis and 34% late apoptosis)[1]. In THP-1 acute monocytic leukemia cells, Pancracine (0.5-200 μM; 72 h) strongly inhibits infection by pseudotyped HIV-1GFP, with an EC50 of 18.51 μM, and inhibition is complete at 100 μM[2].
Cell Proliferation Assay[1]
| Cell Line | human A549 lung adenocarcinoma, MCF-7 breast adenocarcinoma, HepG2 hepatocellular carcinoma, A2780 ovarian carcinoma cells |
|---|---|
| Concentration | 1, 5, 10, 20, 50 μM |
| Incubation Time | up to 96 h |
| Result | Reduced proliferation in all tested cell lines in a concentration-dependent manner. Halted proliferation entirely in A549 cells over the 96-h assay interval at 20 μM. Significantly reduced A549 cell proliferation at 5 and 10 μM. |
Cell Proliferation Assay[1]
| Cell Line | human A549 lung adenocarcinoma, MOLT-4 acute lymphoblastic leukemia cells |
|---|---|
| Concentration | 2.5, 5, 10, 20 μM |
| Incubation Time | 24-72 h (A549); 24-48 h (MOLT-4) |
| Result | Exerted significant antiproliferative effect on A549 cells at 2.5 μM after 48 and 72 h, with increasing effects at higher concentrations. Caused slight decrease in A549 cell viability only at 10 and 20 μM. Exerted significant antiproliferative effect on MOLT-4 cells at 2.5 μM after 24 and 48 h. Reduced MOLT-4 viability significantly at 5 μM after 48 h and at 10 μM after 24 h. Reduced MOLT-4 viability to ~20% at 20 μM. |
Cell Cycle Analysis[1]
| Cell Line | human A549 lung adenocarcinoma cells |
|---|---|
| Concentration | 2.5-20 μM (24 h); 20 μM (48 h) |
| Incubation Time | 24-48 h |
| Result | Caused significant increase in A549 cells in G1 phase at 5 μM after 24 h. Caused significant increase in G1 and G2 phase cells, with concurrent decrease in S phase cells at 20 μM after 24 h. Caused significant increase in G2 phase cells, with reduction in G1 and S phase cells at 20 μM after 48 h. |
Apoptosis Analysis[1]
| Cell Line | human MOLT-4 acute lymphoblastic leukemia cells |
|---|---|
| Concentration | 2.5, 5, 10, 20 μM |
| Incubation Time | 24 h |
| Result | Resulted in early apoptotic rates of 3%, 4%, 10%, and 14% at 2.5, 5, 10, and 20 μM respectively after 24 h. Resulted in late apoptotic rates of 2%, 3%, 14%, and 34% at 2.5, 5, 10, and 20 μM respectively after 24 h. Resulted in 48% total apoptotic cells (14% early, 34% late) at 20 μM after 24 h. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Need this compound in a format that drops straight into your assay? We can tailor formulation, chemistry, and documentation so your results stay consistent across runs and re-orders.
- Format options: solid or pre-dissolved solution (choose solvent), target concentration, aliquots, light/moisture-protected packaging
- Chemistry options: free base/acid vs salt forms, hydrate/solvate preference, stereoisomer control (single enantiomer or racemate), close analogs
- Add-on labels & handles: D/¹³C/¹⁵N isotopes (LC-MS/internal standards), azide/alkyne or other functional handles for conjugation
- QC & documentation: standard COA or enhanced analytical pack (HPLC/LC-MS/NMR), chiral purity, residual solvents, water content (KF), method-specific specs
- Scale & continuity: mg to gram scale, bulk pricing, lot reservation, repeat-order continuity
To quote quickly, tell us: compound name + CAS/structure (SMILES or mol file), intended assay context, solvent preference, salt/stereochemistry requirements, purity/QC level, and the amount (mg–g).
Can’t find the compound you’re looking for?
Send the CAS or structure and your specs. We can help source it, suggest close equivalents, or discuss custom synthesis with the right QC documentation (RUO).
